Cerebromicrocirculatory defects in animal model of depression

Sheldon H. Preskorn, Thomas A. Kent, Robin K. Glotzbach, George H. Irwin, Jay V Solnick

Research output: Contribution to journalArticlepeer-review

12 Scopus citations

Abstract

In the tetrabenazine (TBZ) model of depression, the cerebromicrocirculation was discovered to respond abnormally to metabolic demand as mimicked by the administration of CO2. Altered responsivity of cerebral blood flow and effective permeability of the blood - brain barrier to changes in PaCO2 were found. These physiologic defects coincided temporally with TBZ-induced depletion of central norepinephrine and dopamine and with the development of the behavioral effects of TBZ (the end points used to test the antidepressant potential of experimental drugs). Pretreatment with amitriptyline (a standard antidepressant and amine reuptake inhibitor) prevented the development of these TBZ-induced abnormalities in the cerebromicrocirculation, just as it prevented the behavioral effects.

Original languageEnglish (US)
Pages (from-to)196-199
Number of pages4
JournalPsychopharmacology
Volume84
Issue number2
DOIs
StatePublished - Oct 1984
Externally publishedYes

Keywords

  • Animal model
  • Biogenic amines
  • Bood-brain barrier
  • Cerebral blood flow
  • Depression
  • Tetrabenazine

ASJC Scopus subject areas

  • Pharmacology

Fingerprint Dive into the research topics of 'Cerebromicrocirculatory defects in animal model of depression'. Together they form a unique fingerprint.

Cite this